The research described in this proposal will investigate the molecular mechanisms responsible for the development changes in the nicotinic acetylcholine receptor (nAchR) of the neuromuscular junction. The ultimate goal of this work is to understand the molecular mechanisms by which nerve changes postsynaptic properties. Specific questions that will be addressed are: 1) Are the different properties associated with adult versus embryonic receptors due to expression of different genes? 2) What role does muscle fiber electrical activity play in AchR gene expression? 3) Is adult muscle AchR gene expression localized to endplate nuclei? and 4) In what way do the subunits of the adult or embryonic AchR contribute to the different properties of these receptors? In order to investigate these questions one needs to identify the various AchR gene products expressed during development of the neuromuscular junction. Therefore, the experiments described in this proposal employ the techniques of molecular and cellular biology, muscle cell culture and recombinant DNA and antibody probes for AchR gene products.